Oak leaf (Quercus pyrenaica) poisoning in cattle

Three experiments were conducted to study the clinical and pathological findings associated with poisoning in cattle due to ingestion of young oak leaves (OL) and the main factors responsible for toxicosis. In Experiment 1, six 1.4 year-old bulls were fed up to 5 kg of young OL per animal per day and showed no signs of toxicity, apart from a slight proteinuria. In Experiment 2, another six 1.4 year-old bulls were first subjected to severe feed restriction for eight days and then fed a higher amount of OL (approx. 10 kg) daily. A marked increase of serum creatinine and blood urea (BUN) was detected in urine as well as clinical signs consistent with renal failure. At necropsy, animals showed gastrointestinal ulcers and kidney tubular necrosis. Since these results suggested a crucial role of the feed restricting period, a third experiment was conducted administering the same amount of young OL as in Experiment 1, but adding the severe feed restricting period as in Experiment 2. There was a wide variation in clinical signs, with one bull showing clinical signs and lesions, another recovering after showing mild clinical signs and high levels of creatinine and BUN, and the third appearing clinically normal. The relevance of restriction access to food in the development of OL toxicosis appears to be critical because the intoxication was only elicited when the OL administration was preceded by a severe feed restricting period.     

Cestrum parqui (green cestrum) poisoning in cattle

SUMMARY Naturally occurring cases of poisoning of cattle by Cestrum parqui were characterised by ataxia, depression, recumbency, convulsions and death. Three cattle were dosed experimentally by intrarumenal administration of fresh plant material. One calf died 48 h after receiving 30 g (wet weight) of plant /kg body weight. Doses of 11 and 17 g/kg caused only mild intoxication, with dullness and anorexia lasting 2 days. In natural and experimental cases the main lesion was hepatic periacinar necrosis. Elevated levels of plasma aspartate transaminase and prolonged prothrombin times were demonstrated in experimental cases. Haemorrhage beneath the serosa and into the intestinal lumen occurred in field cases, but not in the experimental. It is concluded that C. parqui poisoning in cattle is a primary hepatotoxicity.     

Bog asphodel (Narthecium ossifragum) poisoning in cattle.

Fifteen cows among a herd of 50 suckler cows and calves rapidly lost body condition and became dull and anorexic after grazing pasture containing bog asphodel (Narthecium ossifragum) during the summer of 1989. The affected cows had evidence of kidney damage characterised by elevated plasma urea and creatinine concentrations. Eleven cows died and diffuse renal tubular necrosis was present in three cows which were examined post mortem. Similar renal lesions were reproduced experimentally by feeding bog asphodel to a healthy calf.     

Nitrogen dioxide (silo gas) poisoning in dairy cattle

Toxic silo gases are a potential danger to livestock housed in close proximity to roughage silos. These gases, such as nitrogen dioxide (NO2), may be produced during the early stages of (maize and grass) silage making. In humans, inhalation of these gases causes a condition known as 'Silo Filler's Disease' (SFD), which is a recognized occupational hazard for workers in upright forage silos in many countries. NO2 accumulates on top of silage, is inhaled by workers, and reacts with water on the airway surfaces to form nitrous acid, which damages the lung and causes pulmonary oedema, bronchiolitis, and death in severe cases. On a dairy farm, a cloud of reddish-brown NO2 gas (which is heavier than air) was noticed to escape from underneath the plastic sheet of a horizontal maize bunker and to enter a cubicle house for dairy cows 1 day after ensiling. Eleven cows became dyspnoeic, 3 of which subsequently died. A combination of weather conditions, an insufficient sand load on the maize bunker, the utilization of a lactobacillus starter culture, and the close proximity of the silo to the cubicle house may have caused the incident.     

Moldy sweet clover (dicoumarol) poisoning in Saskatchewan cattle

Information pertaining to 286 animals from 56 herds affected by moldy sweet clover poisoning in Saskatchewan during 1983 was tabulated from the toxicology laboratory records. The morbidity in the affected herds was 12.1%, with a case fatality of 65.5%. Aborted fetuses and calves less than two weeks of age were affected with sweet clover poisoning most often. Sweet clover poisoning was more common during the period from January to April, 91.6% of the morbid animals were seen at this time. The rates of poisoning in beef and dairy cattle were estimated to be 0.156 and 0.095 cases per 1000 cattle respectively. Sweet clover poisoning was observed with the use of large of small bales of sweet clover in 78.9% of the affected herds. The geographical distribution of sweet clover poisoning in Saskatchewan followed the northern regions of the dark brown soil zone and the southern regions of the black soil zone which extend from the mid northwest portion of the province to the extreme southeast region.

Dicoumarol concentrations were determined on a variety of tissues including liver, plasma, serum, kidney and muscle. Significant differences in the liver dicoumarol concentrations were found between animals of different ages (P = 0.045). Livers from younger animals, in particular, the fetus, contained lower concentrations of dicoumarol.

     

Acute pit gas (hydrogen sulfide) poisoning in confinement cattle.

Rapid deaths in confinement cattle caused by exposure to hydrogen sulfide (H2S) gas from manure pits has not been reported in the USA. In 1997, 158 cattle in 2 confinement pens were exposed to H2S gas as the manure in the pits under a slatted floor was agitated prior to pumping. Approximately 35 of the cattle were lying on the floor when the upper agitator was turned on. Within 5 minutes, many these cattle were down on their sides and paddling. Of these, 26 died within a few minutes. The survivors were treated and sent to slaughter. Cattle that did not show immediate signs of toxicosis remained clinically unaffected. Two steers that were near death were brought to the Purdue Animal Disease Diagnostic Laboratory for clinical evaluation, euthanasia, and necropsy. They were recumbent and unresponsive to visual and auditory stimuli. Necropsy examination yielded no significant gross lesions. No evidence of viral or bacterial infection was found. Ocular fluid nitrate concentrations were within normal limits, and no lead was detected in either animal. Microscopic examination revealed lesions consistent with H2S-induced central nervous system anoxia. Histologically, sections of brain demonstrated massive, diffuse cerebral cortical laminar necrosis and edema. Portions of the outer lamina contained hypereosinophilic and shrunken neurons. The subcortical white matter was vacuolated in some areas. The history, clinical signs, and histologic lesion of cerebral laminar necrosis led to a diagnosis of H2S toxicosis in these cattle.     

Locoweed (Oxytropis sericea) poisoning and congestive heart failure in cattle

Locoweed (Oxytropis sericea), when fed to calves at high elevations, increased the prevalence and severity of congestive heart failure. Forced exercise did not increase the prevalence of congestive heart failure, but it did increase severity. Calves consuming locoweed at high elevations developed signs and gross lesions of congestive heart failure and microscopic lesions of congestive heart failure and locoweed poisoning. Calves fed locoweed at low elevations developed only signs and lesions of locoweed poisoning.